Week 10 (2013)

So, this will be the first of a new style of blogging. I'm not sure how things will turn out, but bear with me. I hope to write a little more so I don't have to immediately vent on Facebook. If I'm still bothered by something at the end of the week, then maybe it really is important. Otherwise, it's in the past. I will also bold face / highlight the beginning of the paragraph so you know what it's about. I know not everyone is interested in my ramblings, so feel free to pick and choose.

[Week 10]
Badminton: 3/5
School: 2/5
Misc: 3/5
OVERALL: 3/5

School has been a bit tough this week, getting some of my midterm grades back from last week, which were disappointing. I also dropped my statistics course as I already had a statistics credit, so hopefully I can use my time wisely to catch up with my other courses and train more. I really have nothing against the course, but I'm pretty sure I did pretty terribly that week on all my midterms. The irony is that I dropped Statistics because I was afraid it would skew my average negatively. I actually don't mind Statistics at all. It helps me understand research papers better, and probabilities are cool too, but I don't think we would be cover it in that class. I went and returned my textbook as well. As I'm now missing a bit of KIN credit, I will be taking a course on coaching in the summer to finish my degree.

In Muscle Physiology (UBC KIN 462), we are starting a new unit on training adaptations. We are highlighting the two extremes, which would be Resistance Training and Aerobic Endurance. I suppose there are parts of both in badminton, but I'm definitely more interested in resistance training. I don't think I've ran more than 20 minutes straight in a very long time, and I don't see why I need to as well. For a Kinesiology course, I find it gets a little too detailed, going into biochemistry and molecular biology. I know it's a Physiology course, but it feels so in depth at times that it's like a Faculty of Science - Physiology course. For example, for hypertrophy (increase in muscle cell size as an effect of resistance training), is a calcium independent pathway due to IGF-1 release, which works through 2 different pathways: 1) The PI3K - Akt pathway [via A) PI3K-Akt-mTOR, B) PI3K-Akt-GSK3B, C) PI3K-Akt-FOXO-MuRF1/MAFbx] and 2) Ras-Raf-MEK-ERK pathway. So you can see that you probably just skimmed through all those letters and acronyms and continued reading here. I don't blame you, but to me, this feels like memory work in a way. It doesn't look too much better on a diagram, but this is what I'm struggling with now I guess. If I didn't take biochemistry, I don't know how I would approach this course. For example, PI3K, is phophatidylinositol 3-kinase, which makes no sense to most people (even in my class). From my biochem class, we actually had to draw the structure of it, so at least I can give a good guess. I'm not going to look it up, but if I had to really guess what it was, it's probably an enzyme that adds a phosphate and is some kind of cell membrane receptor. The structure of phosphatidylinositol is actually kind of close to trigylcerides or triacyglycerols, or... fat! Too many triacylglycerols contribute to that much dreaded body fat that people are constantly trying to lose (albeit a bit too quickly at one, I might say). Regardless, glycerol is a sugar backbone which carries 3 chains of fatty acids, unsaturated or saturated. So, if I remember correctly, phosphatidylinositol has a glycerol back bone, 2 fatty acids, and the 3rd one consists of a phosphate and an inositol, which is kind of like a 6 ringed sugar with a bunch of alcohol groups with some that can be phosphorylated (add phosphate). The term 'kinase' refers to an enzyme that adds a phosphate group to something. ANYWAY... perhaps this level of understanding isn't needed, but it bothers me to just memorize PI3K. Another example, which I haven't researched on is GSK3B. It's not GlaxoSmithKline, and the B stands for Beta. So, is there an... Alpha? Why is it 3? Perhaps I'm going to far...

KIN 462 Notes (Source: Me)

So in my actual Biochemistry class (UBC BIOC 302), we are doing Nucleic Acids now. We did Fats and Proteins for the first midterm, which didn't go so well, so at least it's more of a new start I guess. If I could take a couple sentences to vent about the midterm, it's not that I don't know my stuff. I studied hard for the exam, even with jetlag and all, but I don't know if it wasn't enough, or if all their questions are like 2 scales above the question you typically see. It's like training for a high school or varsity level tournament, and you play against an International level player. Sure, you know the basic concepts, but apply it in THIS situation! Perhaps I need to dig deeper with my studying and know a little more than I'm expected, but I wouldn't know which direction to take. Anyway, that was like a small paragraph, so some cool things we covered were purine and pyramidine synthesis. What are those? Well, what are nucleic acids? They are structures made with a base, a sugar, and a phosphate backbone and it's the structure of your DNA! So, we definitely need the stuff. As you may or may not know, DNA makes RNA, which makes Protein, so it's quite useful stuff. Something which may be more interesting is that the breakdown of the bases (purines) leads to uric acid and elevated levels of uric acid in the blood can lead to gout! Basically, uric acid crystals form in the extremities and cause the surrounding area to be inflamed. So, a treatment that they use in medicine is a chemical called allopurinol which is supposed to be very similar in structure to hypoxanthine, a structure leading to the formation of uric acid. Allopurinol works to compete with hypoxanthine and ends up inhibiting the enzyme xanthine oxidase, which leads to uric acid. By inhibiting the enzyme, less uric acid is made. See, now THAT is cool. Allopurinol is also a treatment for Lesch-Nyhan Syndrome (Juvenile gout) in which there is an HGPRT deficiency due to a genetic condition. And lastly, as a disclaimer, this is biochemistry and NOT medical advice... anywhere on my blog.

(Source: columbia.edu)

Neuroanatomy (UBC KIN 473) was straight forward this week, but that's because we are doing a midterm next Tuesday. I'm not quite ready yet, but I hope to be ready by the end of this weekend (even with a loss of an hour from Daylight Savings "Spring Forward"), and review on Monday. We did a lot more stuff on motor pathways and upper/lower motor neuron lesions in the first midterm, so this time we will be covering more on the ascending sensory pathways and other structures, like the Basal Ganglia. We also covered Parkinson's Disease (PD) for the majority of the previous class which was pretty cool, as we saw a lot of videos on symptoms, treatments, and the Hoehn and Yahr scale which is used to assess the severity of PD symptoms. So, the 4 hallmark symptoms of PD are bradykinesia (slow & small movements), resting tremor (involuntary shaking at rest), rigidity (stiffness caused by increase in muscle tone), and postural instability. Treatment is usually done by trying to replace dopamine levels, as PD is caused by a degeneration of dopaminergic neurons in the Substantia Nigra, a region in the mid-brain. Unfortunately, the brain has this thing called the blood-brain barrier which is very selective on what can go through, so a precursor to dopamine, L-DOPA, is taken instead. L-DOPA looks a lot like the amino acid Tyrosine, which is a non-essential amino acid in the body, only if you are supplementing with Phenylalanine, which would be an essential one. And for those with a genetic defect in converting phenylalanine to tyrosine, you would get someone with Phenylketonuria (PKU). Pretty cool how things tie together, but to finish off with the PD, treatments are very dosage sensitive and there are on-off swings, where 'off' gives severe PD symptoms, and 'on with dyskinesia' leads to some weird abnormal movements. By far the coolest thing I saw about PD, is that a lot of people suffer from 'freezing', where they cannot start a movement. But if there is some type of visual cue, such as a line on the floor to step over, they can actual step over it with their gait looking a lot like normal! See the video:

I've been doing a lot more footwork for my badminton training, hoping to do at least 15-20 mins before every practice. It seems to be helping tremendously in my movement and I've tried a slight adaptation from what I have observed in the movements of some higher level players. In conjunction with a concept I learned in my Neuromuscular Integration class last year, I'm hoping to develop a more explosive, yet stable footwork base for my badminton. It's not anything new, but I hope to make it look and be as effective as some of the Asian players who move in a similar fashion. The connection with my sport science class is that fact that in gait (walking), the point of greatest instability is not when one foot is in mid-air. It is right when the foot comes down and both feet are in contact with the ground in that instant. I think the reason why is because both feet are on the floor at the same time, there is no saving mechanism because the feet are in an unmovable position until the weight transfer is complete. Given that concept, I am trying not to have both feet on the ground at the same time and instead, slow down the speed of my final steps to the center and use it to push off to the next shot instead. A good example of this is watching Alex Pang in the 2013 Canadian Nationals.